flammation. The rat models were randomly assigned to the different treatment groups: acute (48-hour) inflammation, chronic (1-week and 3-week) inflammation, and normal controls. Under anesthesia, endomorphin 1 was injected into the arthritic knee joints of all affected rats. Therapeutic effectiveness was assessed by measures of joint edema formation and sensory nerve activity associated with pain.

In rats with acute arthritis, endomorphin 1 worked to significantly reduce the hypersensitivity of joint nerves by as much as 75 percent. In the rats with chronic arthritis, however, endomorphin 1 had no observable effect on the telltale triggers of pain. On the strength of these findings, researchers concluded that chronic inflammation negates the pain-relieving benefits of the body's u-opioid receptors.

"These observations highlight a possible inadequacy of the endogenous opioid system to alleviate chronic arthritis pain," notes study author Dr. Jason McDougall. By offering clear insights into the disappointment of u-opioid therapy, this study suggests the need for rethinking the best use of endomorphin 1 and redirecting pain management research toward more promising alternatives for long-term arthritis sufferers.

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